Abstract
In order to clarify the peripheral mechanisms of ectopic persistent pain in a tooth pulp following pulpal inflammation of an adjacent tooth, masseter muscle activity, phosphorylated extracellular signal-regulated protein kinase (pERK) and TRPV1 immunohistochemistries and satellite cell activation using glial fibrillary acidic protein (GFAP) immunohistochemistry in the trigeminal ganglion (TG) were studied in the rats with molar tooth-pulp inflammation. And, Fluorogold (FG) and DiI were also used in a neuronal tracing study to analyze if some TG neurons innervate more than one tooth pulp. Complete Freund’s adjuvant (CFA) or saline was applied into the upper first molar tooth pulp (M1) in pentobarbital-anesthetized rats, and capsaicin was applied into the upper second molar tooth pulp (M2) on day 3 after the CFA or saline application. Mean EMG activity elicited in the masseter muscle by capsaicin application to M2 was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats. The mean number of pERK-immunoreactive (IR) TG cells was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats. Application of the satellite cell inhibitor fluorocitrate (FC) into TG caused a significant depression of capsaicin-induced masseter muscle activity and a significant reduction of satellite cell activation. The number of TRPV1-IR TG cells innervating M2 was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats, and that was decreased following FC injection into TG. Furthermore, 6% of TG neurons innervating M1 and/or M2 innervated both M1 and M2. These findings suggest that satellite cell activation following tooth pulp inflammation and innervation of multiple tooth pulps by single TG neurons may be involved in the enhancement of the activity of TG neurons innervating adjacent non-inflamed teeth that also show enhancement of TRPV1 expression in TG neurons, resulting in the ectopic persistent tooth-pulp pain following pulpal inflammation of adjacent teeth.
Highlights
It is well known that ectopic persistent pain is frequently observed in teeth or other intraoral structures following tooth-pulp inflammation [1]
To clarify mechanisms underlying ectopic persistent pulpal pain following tooth-pulp inflammation, we analyzed the masseter muscle activity to evaluate noxious reflex, pERK immunohistochemistry to detect excitable trigeminal ganglion (TG) neurons, glial fibrillary acid protein (GFAP) immunohistochemistry to study satellite cell activation and primary afferent tracings using fluorogold (FG) and DiI applied respectively into M1 or M2 to study the percentage of single TG neurons supplying more than one tooth pulp, and we studied TRPV1 expression TG neurons in rats with Complete Freund’s adjuvant (CFA)-induced tooth-pulp inflammation
It has been reported that Extra cellular-signal regulated kinase (ERK) is phosphorylated in dorsal root ganglion (DRG) neurons following strong noxious stimulation of peripheral cutaneous tissues, and the number of phosphorylated ERK-immunoreactive (pERK-IR) DRG cells increases following increases in stimulus intensity [18]
Summary
It is well known that ectopic persistent pain is frequently observed in teeth or other intraoral structures following tooth-pulp inflammation [1]. The presence of persistent pain in a tooth associated with pulpal inflammation in an adjacent tooth sometimes accounts for misdiagnosis of the source of the persistent pain and inappropriate treatment of non-inflamed healthy teeth. The CNS mechanisms underlying ectopic pain following peripheral inflammation have been reported in many studies [4,5,6,7]. The hyperexcitability of SDH neurons are thought to be involved in neuroplastic changes in the SDH neuronal circuitry following peripheral inflammation that are associated with ectopic persistent pain in the adjacent noninflamed tissues
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
